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Aldosterone is produced from ventricles in patients with essential hypertension
Nobuyasu Yamamoto1, Hirofumi Yasue, Yuji Mizuno
1Division of Cardiovascular Medicine, Kumamoto Aging Research Institute, Kumamoto, Japan.
Insights
Aldosterone is produced in the hearts of patients with essential hypertension, even without left ventricular systolic dysfunction. This cardiac aldosterone production correlates with hypertension severity.
Area of Science:
- Cardiology
- Endocrinology
- Hypertension Research
Background:
- Essential hypertension is a complex condition with various contributing factors.
- The role of cardiac-derived hormones, such as aldosterone, in hypertension is an area of ongoing investigation.
- Left ventricular systolic dysfunction (LVSD) is a known complication of hypertension, but its absence does not preclude other cardiac alterations.
Purpose of the Study:
- To investigate whether aldosterone is produced within the heart of patients with essential hypertension but without left ventricular systolic dysfunction (LVSD).
- To compare cardiac-derived aldosterone levels with systemic levels and correlate them with other cardiovascular markers.
- To explore the relationship between cardiac aldosterone production, angiotensin-converting enzyme (ACE) activity, and blood pressure in hypertensive patients.
Main Methods:
- Cardiac catheterization was performed on 20 patients with essential hypertension (no LVSD) and 22 controls.
- Plasma aldosterone, serum ACE activity, and B-type natriuretic peptide levels were measured from the anterior interventricular vein (AIV), coronary sinus, and aortic root.
- Statistical analyses were used to compare levels between groups and sites, and to assess correlations.
Main Results:
- Hypertensive patients showed significantly higher aldosterone levels in the AIV and coronary sinus compared to the aortic root.
- No significant differences in aldosterone levels were observed at these sites in the control group.
- Aldosterone and ACE activity differences between AIV and aortic root positively correlated with diastolic blood pressure in hypertensive patients.
Conclusions:
- Aldosterone production is activated in the left ventricles of patients with essential hypertension, even in the absence of LVSD.
- Cardiac aldosterone production appears to be proportional to the severity of hypertension.
- These findings suggest a potential role for intra-cardiac aldosterone synthesis in the pathophysiology of essential hypertension.
Abstract:
This study was designed to examine whether aldosterone is produced from the hearts of patients with essential hypertension without left ventricular systolic dysfunction (LVSD). The study population consisted of 20 patients with essential hypertension without LVSD and 22 control subjects. Plasma levels of aldosterone, serum ACE activity, and B-type natriuretic peptide levels were measured in the anterior interventricular vein (AIV), coronary sinus, and aortic root during cardiac catheterization. The plasma aldosterone levels were significantly higher in AIV and coronary sinus than in aortic root (99+/-11 versus 88+/-10 pg/mL, P<0.01, and 100+/-12 versus 88+/-10 pg/mL, P<0.01, respectively) in the hypertension group. On the other hand, there were no significant differences in aldosterone levels for these sites in the control group. There were no significant differences in ACE activity levels between aortic root, AIV, and coronary sinus in either the hypertension or control group. The levels of B-type natriuretic peptide were significantly higher in AIV than in aortic root in both groups. The difference in aldosterone levels between AIV and aortic root (Delta Aldo[AIV-Ao]) had a significant positive correlation with the difference in ACE activity between AIV and aortic root (DeltaACE[AIV-Ao]) (r=0.501, P<0.05) in the hypertension group. Both Delta Aldo[AIV-Ao] and DeltaACE[AIV-Ao] had a significant positive correlation with diastolic blood pressure (r=0.498, P<0.05; r=0.577, P<0.01, respectively) in the hypertension group. We conclude that production of aldosterone is activated in the left ventricles in patients with essential hypertension without LVSD in proportion to the severity of hypertension.